{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T10:46:07Z","timestamp":1786963567993,"version":"build-2736575974"},"reference-count":59,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2021,8,17]],"date-time":"2021-08-17T00:00:00Z","timestamp":1629158400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2021,8,17]],"date-time":"2021-08-17T00:00:00Z","timestamp":1629158400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Fundamemntal Clinical Pharma"],"published-print":{"date-parts":[[2022,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Damage to the peripheral or central nervous system results in neuropathic pain. Based on a complicated mechanism, neuropathic pain has no efficient treatment so far. It has been well\u2010known that the expression of some proteins (BDNF, KCC2, GABA\u2010A) during neuropathic pain changes. Microglial cell activation is considered as a trigger to alter the expression of these proteins. In the current study, the effect of minocycline as a potent microglial activation inhibitor on the gene and protein expression of these neuropathic pain mediators was investigated. This experiment was done in two paradigms, preinjury and postinjury administration of minocycline. In each paradigm, male Wistar rats (weight 150\u2013200\u2009g,\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20096) were allocated to sham, control, and drug groups. Minocycline (30\u2009mg\/kg, i.p.) was injected 1\u2009h before or at day seven after nerve injury and continued till day 14 in the preemptive or postinjury part of the study, respectively. After the last injection, the animals were decapitated and the lumbar part of the spinal cord was isolated to assess the expression of genes and proteins of interest. In the preventive study, minocycline increased the expression of KCC2 and GABA\u2010A\/\u03b3\n                    <jats:sub>2<\/jats:sub>\n                    proteins and decreased BDNF expression. On the other hand, the target gene expression and protein expression were not changed when minocycline was administered after nerve injury. It seems that minocycline was able to change the expression of proteins of interest merely when used before nerve damage.\n                  <\/jats:p>","DOI":"10.1111\/fcp.12719","type":"journal-article","created":{"date-parts":[[2021,7,24]],"date-time":"2021-07-24T06:20:51Z","timestamp":1627107651000},"page":"277-285","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["The effect of microglial inhibition on the expression of BDNF, KCC2, and GABAA receptor before and after the establishment of CCI\u2010induced neuropathic pain model"],"prefix":"10.1111","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0217-439X","authenticated-orcid":false,"given":"Malek","family":"Zarei","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Faculty of Medicine Shahid Beheshti University of Medical Sciences  Tehran 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